Multiple myeloma begins in the bone marrow with plasma cells going haywire. This article shares a multiple myeloma patient story, as well as discusses symptoms and treatment options.
Seven years ago, Tamara Mobley was so busy, active, and energetic that if she were a cartoon, she’d be a blur. The dedicated mother of two young boys, a loving wife and a full-time employee in a good job, she didn’t get much downtime.
“I think I was just busy, like any other typical mom,” Mobley says. “You know, just doing things to take care of the house, my family and doing my best to be a valued employee. That was my life before, just ripping and running.”
Then Mobley, who was 33, got tired. Not just garden-variety, too-little-sleep, I’ve-been-doing-too-much sort of tired. But bone tired, from the moment she woke up each morning. Then, there was the severe back pain. And then, the passing out. She was getting sick and it was happening fast. For a young, vibrant, working wife and mother that was terrifying.
A trip to the emergency room led to a rapid diagnosis of multiple myeloma — a cancer of the blood — and a recommendation from her doctor to seek treatment at Emory and Winship.
Mobley was so ill that she got to Emory University Hospital in an ambulance. And that’s when all the ripping and running slowed way, way down — at least for a while.
Multiple Myeloma Symptoms
As cancer goes, multiple myeloma is a bit of a misfit.
For one thing, it’s rare. The American Cancer Society estimates that about 30,000 new cases of myeloma will be diagnosed this year, trailing far behind the most common cancers — breast and lung — each of which will derail more than 220,000 lives. That’s stiff competition for research funding and awareness.
For another, it’s mysterious. Multiple myeloma begins in the bone marrow with plasma cells going haywire. But experts aren’t entirely sure how the process starts or what the key risk factors are. The disease is most common in people over 65, men are slightly more vulnerable and that African Americans are more than twice as likely as white Americans to get it. But we don’t know why.
The most notable differ
ence between multiple myeloma and pretty much all other types of cancer is that the life expectancy for myeloma patients has doubled in the past decade. All thanks to treatments developed and tested at Emory’s Winship Cancer Institute.
Multiple Myeloma Treatment
Last November, the US Food and Drug Administration (FDA) approved the fourth new myeloma drug to be green-lighted within one year —three of those within one monthv—and all four were tested in clinical trials at Winship.
“There’s no other story like that in cancer,” says Sagar Lonial, Winship’s chief medical officer and chair of the Department of Hematology and Medical Oncology in the School of Medicine.
Since his arrival at Emory and Winship in 1997, Lonial has built the multiple myeloma program into one of the best and most sought-after in the country. A team of experts who specialize in the disease leads this program. As Georgia’s only National Cancer Institute–designated cancer center and one of just 69 in the US, Winship offers patients the chance to be treated in the same building where research is taking place. There are three floors dedicated to basic science and three to clinical care.
“That marriage of research and patient care is powerful,” Lonial says. “Our scientists see cancer patients every day.”
One of those is Mobley, who has been in treatment at Winship since that devastating ambulance ride in 2009. Once her condition was stabilized, she began the standard protocol. It consists of a three-pronged attack:
- Chemotherapy to blast away the cancerous cells
- Stem cell harvesting and transplantation to regenerate healthy bone marrow cells
- Regimen of medications calibrated to keep the cancer at bay and send it into remission for a long time.
It’s that last phase that has put Winship’s approach ahead of other myeloma treatment centers. Instead of a one-by-one, trial-and-error approach to drug therapy, Lonial has advocated a full court press. It allowed to hit the residual cancer with a simultaneous three-drug combination.
Mobley was put on an aggressive course of therapy made up of
- Lenolidamide (Revlimid), an immune modulator
- Bortezomib (Velcade), a proteasome inhibitor
- Dexamethasone, a corticosteroid
“That concept of combination therapy is one that our center is focused on and one that benefited her early on,” Lonial says.
According to myeloma researcher Lawrence Boise, Georgia Cancer Coalition Distinguished Cancer Scholar and coleader of the Cancer Cell Biology Program at Winship, scientists are finding that there are many reasons for this. But the most compelling is that it works. “Dr. Lonial doesn’t leave any bullets in the chamber,” Boise says. “In all the trials, all the data, all the comparisons show that three drugs are better than two.”
When Lonial joined Emory’s hematology and oncology department nearly two decades ago, other researchers might have seen a department struggling with turnover and inadequate resources. With the encouragement of a mentor—Kenneth Anderson, probably the best-known myeloma specialist in the world—Lonial saw an opportunity to build a program, from the ground up.
The bottom floor of Winship houses the Clinical Trials Unit, the key to the multiple myeloma program’s growth and success. Within a few years, Lonial had recruited top scientists and clinicians, including Boise, and was testing new classes of drugs in Phase I clinical trials. They proved to be game changers.
Multiple myeloma is a cancer of the blood that develops when normal, antibody-producing plasma cells become malignant and their growth spirals out of control. They build up in the bone marrow until they crowd out healthy blood cells. They can form lesions and tumors in multiple bones, hence the condition’s name.
But the cancerous cells also secrete protein and, like normal cells, they’re engineered to do this in a particular way—the protein assembled and folded just so. When that assembly goes awry, as it does in myeloma cells, the malformed proteins are broken down by proteasomes—protein complexes whose job it is to get rid of problem proteins by degrading them—and that opens up the pipeline for more myeloma cell production.
About ten years ago, scientists discovered that if you interfere with the proteasome’s work—allowing the abnormal proteins to accumulate—the cancerous cells, which in a sense are trying to function normally, will self-destruct. Rapidly.
“Proteasome is part of quality control, so if you inhibit that, and all these mid-folded proteins build up, that causes stress, and the cell kills itself,” Boise explains.
Winship conducted trials of a promising proteasome inhibitor, bortezomib (Velcade), in 2002. One of the first patients to receive it went into remission quickly. “If there was a moment when the light went on, it was then. I remember running upstairs to the director’s office with the graph of this patient’s counts,” Lonial says. “That treatment is now the standard of care.”
Learn more about Tamara’s story here.